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Effect of aging in
CARDIO-PULMONARY SYSTEM
Krishna priya
?
PHYSIOTHERAPY - AGING
 Physiological changes
 Exercise prescription
 Exercise response
 Factors affecting aging – biological and psychological
factors, disuse, disease etc…….
SAFETY OF THE CLIENT DURING REHABILITATION
ANATOMICAL -
 Increase in heart weight
 Decrease in myocardial cells and enlargement of
remaining cells
Cardio-vascular system
 Increased left ventricular thickness
 Increase in left atrial size
 Reduced elastin and increased collagen in the intimal
layer of the heart and blood vessel walls and
calcification stiffness
 Decreased aortic distensibility
 Stiffness increase in systolic blood pressure
 Decreased distensibility increased load on LV
AT REST
Diastolic properties
EDV in cardiac cycle -
 Sufficient venous return
 Relaxation of ventricles
 Duration of atrial contraction
 Inspite of the stiffness if the walls, LA increase in size
maintains EDV
Relation between anatomical and
physiological changes
 Increase in iso-volumic myocardial relaxation
 Decrease in ventricular filling rate in early diastole
 Over all increased diastole of ventricles
DURING ACTIVITY OR MINIMAL EXERCISE
 EDV index increases
 Ventricular filling rate decreases due to prolonged
relaxation time and ventricular stiffness
AT REST
Systolic properties
 End systolic volume
 Stroke volume same
 Ejection fraction
DURING ACTIVITY OR MINIMAL EXERCISE
 End systolic volume
 Ejection fraction
 Myo-cardial contractility
Causes –
 Decreased response to B-adrenergics
 Systolic BP
 Ventricular wall changes
AEROBIC CAPACITY
 VO2 max
 As age VO2 max
 0.4-0.5 ml/kg/min/yr – male
 0.2-0.35 ml/kg/min/yr – female
 10% per decade
 VO2 max inversely proportional to body weight and
physical inactivity
Causes –
 Maximum HR
 CO and SV
 A-V O2 difference
OTHER CHANGES
 Reduced baro receptor and cardio pulmonary reflexes
 Reduced A-V dilatation
 Postural hypotension
Diastole –
 Left ventricular wall thickness
 Left ventricular filling rate
 End diastolic volume
Systole –
 Myocardial contractility
 End diastolic volume
 Ejection fraction
Effect of aging
 Arterial wall thickness
 Systolic blood pressure
 Diastolic blood pressure
 Orthostatic tolerance
 Arterial and venous dilation
 Vasoconstriction
same
 Cause peripheral effects not central
 HR max cannot be changed so SV, CO, VO2 max cannot
be altered significantly
 Extraction of O2 by peripheral skeletal musculature
 A-V O2 difference
VO2 max increases
 EDV at rest and exercise
 Peak rate of ventricular filling
Effect of exercise training on CVS
 6 months – avg- 30 min, 3 times/week, 4-6 months –
increased VO2 max by 14%
 Active / sedentary – VO2 max reduces
(5%) (10%)
Poor improvements in
 Less initial VO2 max
 Increased age
 Short sessions of exercises
 Short over all duration of the study period
Study –
60-82 yrs, intensive endurance training,
Increase in EDV and peak ventricular filling rates
Causes
 Increased uptake of Ca
 Reduced relaxation time
 Increased fatty acid oxidation and cytochrome C
oxidase levels
Systolic performance
 Increased exercise stroke volume,
 Increased ejection fraction, on exercise
 End systolic volume decrease
Very old age, estrogen deficient women – no changes
on exercise training
 Improvement in postural hypotension – blood flow to
peripherally active muscles from inactive limbs and
viscera
 Reduce systolic and diastolic BP
 Reduce age related baro-reflex sensitivity
 Alters ANS and its control on resting HR
 Increase para-sympathetic activity and attenuates
sympathetic activity
Long term aerobic training -
 Decrease symp + at given work rate
 Decrease exe HR
 Decrease BP
Diastole – on exercise
 Left ventricular wall thickness
 Left ventricular filling rate
 End diastolic volume
Systole –
 Myocardial contractility
 End diastolic volume
 Ejection fraction
Effect of exercise training
 Arterial wall thickness ?
 Systolic blood pressure
 Diastolic blood pressure /
 Orthostatic tolerance ?
 Arterial and venous dilation ?
 Vasoconstriction
 Central venous pressure ?
PULMONARY SYSTEM
Anatomical changes – (thoracic cage, lungs, diaphragm)
decreased –
 Calcification of costal cartilage with sternum
 Degenerative changes in thoracic spine and rib
articulations
 Kyphosis
 Reduced intervertebral spaces, Wedge shaped
 Increases AP diameter
 Resp muscles in mechanically disadvantageous position
 Decreased force generation
 Loss of elastic fibres in alveolar ducts
 Loss and destruction of supporting structures of lung
parenchyma
 Pre-mature closure of airways
Hyper-inflation
 Elastic recoil
 chest wall compliance
 Progressive decrease in respiratory muscle strength
(mild)
 Compliance – lung and chest wall
 Decrease in chest wall complian
-ce is more than lung compliance
Decrease in
 Alveolar – capillary surface area
 Alveolar surface area
 Total surface area of lung parenchyma
 Pulmonary blood flow volume
 Reduced diffusion
 Increased dead space ventilation
 V/Q mis-match
 Reduced elastic recoil – reduced exp flow + narrowing
of airways
Reduced FEV1
 Reduced closing volumes, increased FRC and RV
Reduced FVC and flow rates
 Increased FRC TV decreases
 Minute ventilation –RR*vol of air inhaled in 1 breath
 Increase in RR, inspite of TV inspiration
 Diaphragm – change in muscle type – reduced type 1
muscle fibres
Easy fatigue during increased load on RS
Increased WOB
Immunological changes –
 BAL – broncho alveolar lavage
 Increased neutrophils; IgA, IgM,
 Reduced macrophages
 Antigens toxin production
Increased T lymphocytes
Increased neutrophils
Release of super-oxide
Persistent low grade inflammation
Damage to lung matrix
Impaired gaseous exchange
 ELF- epithelial lining fluid – rich in anti-oxidants
Aging – reduced ELF
Increased susceptibility to env toxins
25-35/40 yrs (plateau)
Growth and maturation declines
0-20 yrs
Pulmonary changes also depend on -
nutrition / diet
life style – sedentary/active, smoking
infections, environment
immune system
 Chest wall stiffness
 Elastic recoil
 Alveolar capillary surface area
 Forced expiratory flow
 Total residual volume
 Forced vital capacity
 P I max and P E max
 V/Q matching
 Pa O2
 Oxygen saturation
 Pulmonary vascular resistance
Effect of aging
 Expiratory flow limitation
 Minute ventilation
 Work of breathing
 Resp muscle O2 consumption
 Pulmonary artery pressure
DURING ACTIVITY OR MINIMAL EXERCISE
 Expiratory flow limitation due to narrow air ways
 Increase in minute volume, minimal increase in TV,
more in RR, shortness of breath
 Increased WOB to meet O2 demands via alveolar
ventilation, diffusion
 Exe – stiff alveolar walls – reduced elastic recoil-
increase pressure development by insp and exp
muscles – increased WOB – increased O2 consumption
by resp muscles (10-12% of total body O2 consumption)
Sub-maximal exe – aerobic training – MV
 Walking, 70 yr, 12 week sub-maximal aerobic exe, 7.7%
in MV
 Reduced breathlessness
 Low exertion
 Use of low % of max ventilatory capacity during
exercise (reduced WOB)
Effect of exercise training
Maximal exercise – 5 days/ week, 78% HR max
 Same case 14% in max MV
 Improved MV in terms of TV not RR
aging on exercise
 Expiratory flow limitation
 Minute ventilation S M
 Work of breathing
 Resp muscle O2 consumption
 Arterial hypoxemia
 Pulmonary artery pressure
 Pulmonary wedge pressure
Effect of exercise training
Thank You

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EFFECT OF AGING ON CARDIO-PULMONARY SYSTEM

  • 1. Effect of aging in CARDIO-PULMONARY SYSTEM Krishna priya
  • 3.  Physiological changes  Exercise prescription  Exercise response  Factors affecting aging – biological and psychological factors, disuse, disease etc……. SAFETY OF THE CLIENT DURING REHABILITATION
  • 4. ANATOMICAL -  Increase in heart weight  Decrease in myocardial cells and enlargement of remaining cells Cardio-vascular system
  • 5.  Increased left ventricular thickness  Increase in left atrial size  Reduced elastin and increased collagen in the intimal layer of the heart and blood vessel walls and calcification stiffness  Decreased aortic distensibility
  • 6.  Stiffness increase in systolic blood pressure  Decreased distensibility increased load on LV AT REST Diastolic properties EDV in cardiac cycle -  Sufficient venous return  Relaxation of ventricles  Duration of atrial contraction  Inspite of the stiffness if the walls, LA increase in size maintains EDV Relation between anatomical and physiological changes
  • 7.  Increase in iso-volumic myocardial relaxation  Decrease in ventricular filling rate in early diastole  Over all increased diastole of ventricles DURING ACTIVITY OR MINIMAL EXERCISE  EDV index increases  Ventricular filling rate decreases due to prolonged relaxation time and ventricular stiffness
  • 8. AT REST Systolic properties  End systolic volume  Stroke volume same  Ejection fraction DURING ACTIVITY OR MINIMAL EXERCISE  End systolic volume  Ejection fraction  Myo-cardial contractility
  • 9. Causes –  Decreased response to B-adrenergics  Systolic BP  Ventricular wall changes AEROBIC CAPACITY  VO2 max  As age VO2 max  0.4-0.5 ml/kg/min/yr – male  0.2-0.35 ml/kg/min/yr – female  10% per decade
  • 10.  VO2 max inversely proportional to body weight and physical inactivity Causes –  Maximum HR  CO and SV  A-V O2 difference OTHER CHANGES  Reduced baro receptor and cardio pulmonary reflexes  Reduced A-V dilatation  Postural hypotension
  • 11. Diastole –  Left ventricular wall thickness  Left ventricular filling rate  End diastolic volume Systole –  Myocardial contractility  End diastolic volume  Ejection fraction Effect of aging
  • 12.  Arterial wall thickness  Systolic blood pressure  Diastolic blood pressure  Orthostatic tolerance  Arterial and venous dilation  Vasoconstriction same
  • 13.  Cause peripheral effects not central  HR max cannot be changed so SV, CO, VO2 max cannot be altered significantly  Extraction of O2 by peripheral skeletal musculature  A-V O2 difference VO2 max increases  EDV at rest and exercise  Peak rate of ventricular filling Effect of exercise training on CVS
  • 14.  6 months – avg- 30 min, 3 times/week, 4-6 months – increased VO2 max by 14%  Active / sedentary – VO2 max reduces (5%) (10%) Poor improvements in  Less initial VO2 max  Increased age  Short sessions of exercises  Short over all duration of the study period
  • 15. Study – 60-82 yrs, intensive endurance training, Increase in EDV and peak ventricular filling rates Causes  Increased uptake of Ca  Reduced relaxation time  Increased fatty acid oxidation and cytochrome C oxidase levels
  • 16. Systolic performance  Increased exercise stroke volume,  Increased ejection fraction, on exercise  End systolic volume decrease Very old age, estrogen deficient women – no changes on exercise training
  • 17.  Improvement in postural hypotension – blood flow to peripherally active muscles from inactive limbs and viscera  Reduce systolic and diastolic BP  Reduce age related baro-reflex sensitivity  Alters ANS and its control on resting HR  Increase para-sympathetic activity and attenuates sympathetic activity
  • 18. Long term aerobic training -  Decrease symp + at given work rate  Decrease exe HR  Decrease BP
  • 19. Diastole – on exercise  Left ventricular wall thickness  Left ventricular filling rate  End diastolic volume Systole –  Myocardial contractility  End diastolic volume  Ejection fraction Effect of exercise training
  • 20.  Arterial wall thickness ?  Systolic blood pressure  Diastolic blood pressure /  Orthostatic tolerance ?  Arterial and venous dilation ?  Vasoconstriction  Central venous pressure ?
  • 22. Anatomical changes – (thoracic cage, lungs, diaphragm) decreased –  Calcification of costal cartilage with sternum  Degenerative changes in thoracic spine and rib articulations  Kyphosis  Reduced intervertebral spaces, Wedge shaped  Increases AP diameter  Resp muscles in mechanically disadvantageous position  Decreased force generation
  • 23.  Loss of elastic fibres in alveolar ducts  Loss and destruction of supporting structures of lung parenchyma  Pre-mature closure of airways Hyper-inflation  Elastic recoil  chest wall compliance  Progressive decrease in respiratory muscle strength (mild)
  • 24.  Compliance – lung and chest wall  Decrease in chest wall complian -ce is more than lung compliance
  • 25. Decrease in  Alveolar – capillary surface area  Alveolar surface area  Total surface area of lung parenchyma  Pulmonary blood flow volume  Reduced diffusion  Increased dead space ventilation  V/Q mis-match
  • 26.
  • 27.  Reduced elastic recoil – reduced exp flow + narrowing of airways Reduced FEV1  Reduced closing volumes, increased FRC and RV Reduced FVC and flow rates  Increased FRC TV decreases
  • 28.
  • 29.  Minute ventilation –RR*vol of air inhaled in 1 breath  Increase in RR, inspite of TV inspiration  Diaphragm – change in muscle type – reduced type 1 muscle fibres Easy fatigue during increased load on RS Increased WOB
  • 30. Immunological changes –  BAL – broncho alveolar lavage  Increased neutrophils; IgA, IgM,  Reduced macrophages  Antigens toxin production Increased T lymphocytes Increased neutrophils Release of super-oxide
  • 31. Persistent low grade inflammation Damage to lung matrix Impaired gaseous exchange  ELF- epithelial lining fluid – rich in anti-oxidants Aging – reduced ELF Increased susceptibility to env toxins
  • 32. 25-35/40 yrs (plateau) Growth and maturation declines 0-20 yrs Pulmonary changes also depend on - nutrition / diet life style – sedentary/active, smoking infections, environment immune system
  • 33.  Chest wall stiffness  Elastic recoil  Alveolar capillary surface area  Forced expiratory flow  Total residual volume  Forced vital capacity  P I max and P E max  V/Q matching  Pa O2  Oxygen saturation  Pulmonary vascular resistance Effect of aging
  • 34.  Expiratory flow limitation  Minute ventilation  Work of breathing  Resp muscle O2 consumption  Pulmonary artery pressure
  • 35. DURING ACTIVITY OR MINIMAL EXERCISE  Expiratory flow limitation due to narrow air ways  Increase in minute volume, minimal increase in TV, more in RR, shortness of breath  Increased WOB to meet O2 demands via alveolar ventilation, diffusion  Exe – stiff alveolar walls – reduced elastic recoil- increase pressure development by insp and exp muscles – increased WOB – increased O2 consumption by resp muscles (10-12% of total body O2 consumption)
  • 36. Sub-maximal exe – aerobic training – MV  Walking, 70 yr, 12 week sub-maximal aerobic exe, 7.7% in MV  Reduced breathlessness  Low exertion  Use of low % of max ventilatory capacity during exercise (reduced WOB) Effect of exercise training
  • 37. Maximal exercise – 5 days/ week, 78% HR max  Same case 14% in max MV  Improved MV in terms of TV not RR
  • 38. aging on exercise  Expiratory flow limitation  Minute ventilation S M  Work of breathing  Resp muscle O2 consumption  Arterial hypoxemia  Pulmonary artery pressure  Pulmonary wedge pressure Effect of exercise training